Maisarah Repin

SEPSIS (Lecture 17/2/10) Before fever, there are 3 types of changes of fever that is
called pre-sepsis : 1° purulent focus
= systemic disease triggered by special kind of infectious,
endogenic microorganisms and characterised by prolonged 1. Short time 1-day ↑ of temperature during 1-2
unrestricted hyperaemia with hemodynamic abnormalities weeks
and end-organ failure 2. 2-3 days period of high fever during some weeks
3. Undulant fever last 3-4 weeks
Main peculiarities : There is no cyclic course (dt unrestricted)
Fever
Septicemia Bacteremia - can be hectic or remittent
Triggered by special kind of Isolation of bacteria from - Hectic is a difference of temperature > 2 C
infection, so called endogenic peripheral blood & mb - Remittent is a difference of temperature between 1 – 2 C
microorganism transient or
inconsequential Toxicosis
Char by unrestricted May progress to septic - Shaking chills
bacteremia, hemodynamic shock if unRx - HA
dist n organ F - Prostration
Cause by conditional Cause : absolute - n+v
pathogen, colonizing human pathogenic microbe
body after procedure(abortion,
Enlarged spleen
skin abrasion)
- HSM  early symptom. Develop in the first few days of
disease
- USE can reveal it in the beginning and after some time, it
ETIOLOGY can be revealed by palpation.
- Structure of liver is soft, sagging and painless
– Can be caused by a lot of commensals
– They colonize human body since neonatal period, Changes in blood
during which time immune mechanisms are absent. - ↑ leukocytes
They colonize mucosa of the respiratory tract, GIT and - Neutrophils have toxic granularities
co-exist with microorganism - TCP
– Play a great role -> Immunogenic readiness to defend - ESR
organism against pathogenic microbes - anemia at later terms of disease
Causes: Hemorrhagic rash  symptom of generalized vasculitis
 range from point elements to extensive
• Gram –ve  Proteus, Klebsiella, Enterobacter,
Bacteriods (Cl. Perfringens) Primary purulent foci
• Gr. +ve  Staphylococcus, Streptococcus
 Not obligate sign of sepsis
Sometimes the microbe associated may cause sepsis  Local inflammation
 X always the SOI
PATHOGENESIS  Trigger factor
 Their sanation don’t lead to restriction of sepsis
Main factor : breakdown of defence mechanism against
commensals & generalisation of endogenous infection Secondary purulent foci

Develop typical pathologic process  = progressive disease

↓  Characterised by metastatic foci (abscess,
Septic vasculitis phlegmona, meningitis, endocarditis)
 Sign of poor prognosis, will lead to multiple organ-
failure, which is the final stage with high auto-
○ Paresis of blood vessels and nerves
immune process and auto-aggression
which lead to fulminant sepsis and ITS
○  permeability & output of fluid from Multiple Organ Failure is the final stage of the disease that
blood to surrounding tissue. This lead to often leads to death and is characterised by high auto-
high doses of BAS, Inflammatory immune process and auto-aggression. It is associated with:
Cytokines, transformation of tissue
protein to autoAg.  Heart failure
○ Auto-aggression is triggered  Renal failure
 Respiratory failure
Auto-aggression = 2° inflammatory foci formed in diff organs
Respiratory failure is dt lung damage and progressive acute
 respiratory failure or non-cardiac pulmonary edema (shock
lung)
Progress and lead to development of multi-organ failure
Renal failure is characterised by oliguria, proteinuria and 
↓ BUN. It develops in the first 3 days.

They are reflected in main CM of sepsis (cardinal Sx) : SHOCK

(1) Fever -variant of hypertoxicosis at the 1st day/hours of sepsis

(2) Toxicosis -maybe as complication of a final stage of the disease
(3) Enlarged spleen -characterized by hemodynamic disorders as a result of
(4) Blood test changes toxin’s action(vasodilatation) & development of septic
(5) Hv 1° and 2° foci vasculitis
(6) Multi-organ failure & death There are 3 stages of shock according the mechanism of
compensation :
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1. Compensated Positive result may be estimated in 5-7 days

- support BP Negative results are in 10-14 days
- make up blood circulating volume
- catecholamines lt spasm of pre-capillary TREATMENT
sphincter – Should be aggressive
-  BP but ↓ in amount of capillaries. – Antimicrobial therapy
- centralization of blood circulation ○ Best should be on result of sensitivity
test but its not clinically responsible
because it takes a long time
2. Subcompensated ○ Odontogenous :
- paresis of pre-capillaries  Ampiox (Ampicillin +
- ↓ of catecholamines Oxacillin)
- congestion of blood in venous part
- ↓ venous return, ↓ systolic CO
 3rd generation Cephalosporin
○ Tonsillogenous
 Ampiox
3. Decompensated  Aminoglycosides
- there is absence of perfusion ○ All others
- ↑ in lactate and leads to peripheral acidosis  Aminoglycoside
-  in breathing (dyspnea, tachypnea) leads to  Cephalosporin
central alkalosis
- STOP in metabolism and death ensues General rule is we should use a combination of 2 Antibiotics
in maximal dose and one of the doses must be in IV form.
We must estimate efficacy in 24hours. If there is no
improvement, change the antibiotic.
CLASSIFICATION
Anticoagulants
1. Origin – Max dose
a. Otogenic Staphylococcal – Constantly during the day
– 20 000 – 80 000 U of Heparin
b. Odontogenic  Anaerobes
c. Tonsillogenic  Streptococcal Protease inhibitor
– Prevent auto-aggression
d. Urinogenous  Gram –ve bact ○ Octreatid
e. Obstetrical origin  Anaerobes ○ Gordox
f. Intestinal origin  E.Coli
Immunotherapy

2. Modern classification, in use since 1991 Extracorporal detoxication

– Not to be started during active phase because it ↓
Bacteremia +ve hemoculture without CM, concentration of antibiotic
revealed at special Ix – Exception for septic shock or severe sepsis

Syndrome of systemic w/o bacterial confirmation DDX

inflammatory reaction Fever >38.5 or <35.6, BP
<90mmHg, PR > 90bpm Typhoid or Paratyphoid
dyspnea > 20/min, oliguria, Epidemic typhus
leukocytosis > 12 Malaria
HIV

Sepsis CM + Lab confirmation If  epidemic data of contact with animals, then suspect :
– HFRS
Severe sepsis CM + forming of 2° purulent foci, – Yersiniosis
poor prognosis and  risk of – Brucellosis
death
Differential diagnosis with non-infectious disease
Outcome = Septic Shock – Collagenosis
○ Different temperature curve, in this case
3 types of Sepsis : it is not ‘correct’ fever, for example high
1. Fulminant fever for 2 -3 days then no fever for a
2. Acute ( >3 days) few days then again fever…
3. Chronic (>1.5 months) ○ In spite of high fever, ↓ leukocytes
○ Oral steroids are effective
DIAGNOSIS – Tuberculosis
○ Fever, x like sepsis
- Bacteria isolated from blood ○ We don’t see typical changes of blood
There are a few techniques on how to obtain blood
○ +ve skin test (Mantoux test)
specimen
• Site of venopuncture must be disinfected ○ APR
• Blood should be drawn at 2 different sites – Pathology of blood
• Multiple samples should be drawn (3 samples over ○ Myeloleucosis
a 24h period)  Fever + hemorrhagic syndrome
• Blood should be drawn before antibiotics – Tumors with metastasis
administration – Post-vaccination reaction
○ Difficult because fever precede vaccine
The best period to take samples is during chills period 10 – 15 days
because this means there is output of bacteria into the blood – Schizophrenia
stream. The period of max temperature signifies the release ○ Have hallucinations, thought echo, etc
of pyrogens after bacteria destruction.
Chronic Sepsis must be differentiated with
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– TB
– Pathology of thyroid gland
– Encephalic symptoms (febrile for months)